The Right Ventricle in Chronic Pressure Overload: Identifying Novel Molecular Targets for Functional Imaging

Chronically elevated pulmonary pressures do not immediately result in right ventricular failure. During the initial period of exposure, the RV adapts to the increased afterload by altering its metabolism and morphology so as to meet the increased work requirement. Several, interconnected adaptive mechanisms have been proposed, including myocyte hypertrophy, a switch in the primary fuel used for ATP generation, increased angiogenesis, and decreased production of mitochondrial reactive oxygen species. While adaptation is initially successful in many cases, it is temporary, and after an uncertain period of time, the ventricle begins to fail. This transition from a compensated to decompensated state is difficult to predict clinically, and patients with different etiologies of CPOS progress to overt RV failure over significantly different time periods. This variability hinders the implementation of treatments that are tailored to a specific disease stage.